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Abstract

Vasa vasorum (VV) are small arterial and venous networks that originate from major arteries and drain into major veins; penetrating into the arterial wall to supply oxygen and nutrition for the tissues on the outer layer of the vessel walls and draining the by-products of metabolism. In the case of atherosclerosis, VV may grow into the plaque and supply the cells inside, which contribute to the progression of atherosclerosis and increase the risk of future plaque rupture. Additionally, VV could also be a source of intraplaque pressure that inflates the plaque when the luminal pressure decreases below a certain threshold during the cardiac cycle. Such cyclic inflations could pose another risk factor of a vulnerable plaque as the dynamics during inflations could weaken the caps of plaque. A sudden change between the intraplaque pressure and the luminal pressure would incur more inflation stress on the plaque cap and thus increase the likelihood of plaque rupture. Therefore, the density of VV within an atherosclerotic plaque could be an important factor to estimate the vulnerability. Ultrasound strain imaging is a technique that can be used to measure non-invasively how much a plaque inflates during a cardiac cycle, which could be associated with the volume of VV inside the plaque. In addition, the peak-systolic velocity (PSV) within the stenosis affects the plaque inflation due to the Bernoulli Effect. The work in the thesis focuses on a pilot study to research how the carotid plaque inflates among carotid atherosclerosis patients with ultrasound strain imaging, and relates the inflation with the PSVs measured by spectral Doppler. 22 carotid stenosis cases were studied and the results show that most carotid plaques inflate during cardiac cycle, and inflations correlate with PSV. The results provide encouraging evidence to the VV inflation hypothesis and pave the path to future in-depth research on larger population of patients.